Alcohol is a well-recognized human teratogen. In general, the greater the amount consumed by the pregnant woman, the greater the risk of damage to the fetus. Furthermore, the amount of alcohol consumed before a woman knows she is pregnant correlates better with the fetal effects than the amount of drinking midway through pregnancy. Unfortunately, experience from interviewing women during pregnancy has shown that underreporting of the amount consumed is common. Hence, there has been a need for a reliable biologic marker that could identify early the high-risk mother, who could be counseled to change her drinking behavior, or that could provide reassurance to the worried pregnant woman concerned about her drinking before she knew she was pregnant. Hemoglobin-associated acetaldehyde (HbAA) has been developed as an assay for the metabolic by-product of alcohol dehydrogenase, acetaldehyde. In adult volunteers, the blood level of HbAA continued to show residual evidence of alcohol throughout a 28 day study, following the consumption of 0.3gms/kg (about 1 to 2 glasses of wine) only on the day 0 of the study. The proposed pilot study would be the first evaluation of HbAA as a potential marker of previous alcohol consumption in pregnant women. Growth retardation and microcephaly are the most common effects of prenatal exposure to an excessive amount of alcohol. The recognizable craniofacial effects of alcohol correlate with prenatal exposure to very high amounts. We propose to determine the frequency of four outcomes: microcephaly, growth retardation, major malformations, and the facial features attributed to fetal alcohol exposure. The infant's head size and length will be adjusted for mid-parent head size and height. Confounders to be considered are cigarette smoking and cocaine use; by- products will be measured in maternal serum (cotinine) and urine samples during pregnancy. Power calculations show that, with the expected rate of alcohol use of 25% in pregnancy, the power to detect a doubling of the 3% frequency of growth retardation among alcohol users is 0.92. During this pilot study we will also investigate the suggestion that the alcohol- damaged infants are more likely to have certain alleles of alcohol dehydrogenase (ADH). Methods will be developed for establishing the ADH genotype on tissues readily available in newborn infants, such as epithelial cells swabbed from the buccal mucosa.